TBD Meeting (4948-17)

WASHINGTON – Normalizing vitamin D levels correlated with lower insulin resistance and decreased adipose fibrosis in obese patients, according to a study presented at the Eastern regional meeting of the American Federation for Medical Research.

Approximately 86 million U.S. patients have prediabetes, according to Diabetes Report Card 2014, the most recent estimates from the Centers for Disease Control and Prevention. Vitamin D therapy may be able to help lower that number and prevent diabetes in some patients, Jee Young You, MD, a research fellow at Albert Einstein College of Medicine, New York, said at the meeting.

“When there’s increased adiposity, there is reduction of the blood flow which will further lead to inflammation, macrophage infiltration, and fibrosis, which all together leads to insulin resistance,” Dr. You said. “It is shown that there are vitamin D receptors present on adipocytes, so we hypothesize repleting vitamin D will help in reducing this inflammation.”

In a double blind study, Dr. You and her colleagues randomized 11 obese patients, with an average body mass index of 34 kg/m2, insulin resistance, and vitamin D deficiency to vitamin D repletion therapy. Eight similar patients served as controls. The average age was 43 years.

Patients in the test group were placed on a step schedule for vitamin D supplementation. For 3 months, they received 40,000 IU of vitamin D3 weekly in an effort to reach a target 25-hydroxyvitamin D level of greater than 30 ng/ml. Patients then received another 3 months of the same supplementation with an aim to reach a target level of greater than 50 ng/ml.

“We wanted to see if there was a dose dependent effect for vitamin D in patients,” Dr. You said.

Endogenous glucose production decreased by 24% (P = .04) after normalization of vitamin D levels. Patients who received placebo saw an increase in endogenous glucose, pointing to lower hepatic insulin sensitivity, Dr. You said.

When the vitamin D receptors are activated, they inhibit the profibrotic pathways like TGFb-1, Dr. You explained, decreasing fibrosis.

The researchers also found a decrease in profibrotic gene expression in TGFb-1, HiF-1, MMP7, and Collagen I, V, and VI.

However, while testing for reduction in profibrotic gene expression in whole fat, the investigators found that there was no additional improvement after the first round of vitamin D therapy, leading them to assert that raising vitamin D levels above the normal range does not give any additional benefit.

ezimmerman@frontlinemedcom.com

On Twitter @eaztweets

WASHINGTON – Normalizing vitamin D levels correlated with lower insulin resistance and decreased adipose fibrosis in obese patients, according to a study presented at the Eastern regional meeting of the American Federation for Medical Research.

Approximately 86 million U.S. patients have prediabetes, according to Diabetes Report Card 2014, the most recent estimates from the Centers for Disease Control and Prevention. Vitamin D therapy may be able to help lower that number and prevent diabetes in some patients, Jee Young You, MD, a research fellow at Albert Einstein College of Medicine, New York, said at the meeting.

“When there’s increased adiposity, there is reduction of the blood flow which will further lead to inflammation, macrophage infiltration, and fibrosis, which all together leads to insulin resistance,” Dr. You said. “It is shown that there are vitamin D receptors present on adipocytes, so we hypothesize repleting vitamin D will help in reducing this inflammation.”

In a double blind study, Dr. You and her colleagues randomized 11 obese patients, with an average body mass index of 34 kg/m2, insulin resistance, and vitamin D deficiency to vitamin D repletion therapy. Eight similar patients served as controls. The average age was 43 years.

Patients in the test group were placed on a step schedule for vitamin D supplementation. For 3 months, they received 40,000 IU of vitamin D3 weekly in an effort to reach a target 25-hydroxyvitamin D level of greater than 30 ng/ml. Patients then received another 3 months of the same supplementation with an aim to reach a target level of greater than 50 ng/ml.

“We wanted to see if there was a dose dependent effect for vitamin D in patients,” Dr. You said.

Endogenous glucose production decreased by 24% (P = .04) after normalization of vitamin D levels. Patients who received placebo saw an increase in endogenous glucose, pointing to lower hepatic insulin sensitivity, Dr. You said.

When the vitamin D receptors are activated, they inhibit the profibrotic pathways like TGFb-1, Dr. You explained, decreasing fibrosis.

The researchers also found a decrease in profibrotic gene expression in TGFb-1, HiF-1, MMP7, and Collagen I, V, and VI.

However, while testing for reduction in profibrotic gene expression in whole fat, the investigators found that there was no additional improvement after the first round of vitamin D therapy, leading them to assert that raising vitamin D levels above the normal range does not give any additional benefit.

ezimmerman@frontlinemedcom.com

On Twitter @eaztweets

WASHINGTON – Normalizing vitamin D levels correlated with lower insulin resistance and decreased adipose fibrosis in obese patients, according to a study presented at the Eastern regional meeting of the American Federation for Medical Research.

Approximately 86 million U.S. patients have prediabetes, according to Diabetes Report Card 2014, the most recent estimates from the Centers for Disease Control and Prevention. Vitamin D therapy may be able to help lower that number and prevent diabetes in some patients, Jee Young You, MD, a research fellow at Albert Einstein College of Medicine, New York, said at the meeting.

“When there’s increased adiposity, there is reduction of the blood flow which will further lead to inflammation, macrophage infiltration, and fibrosis, which all together leads to insulin resistance,” Dr. You said. “It is shown that there are vitamin D receptors present on adipocytes, so we hypothesize repleting vitamin D will help in reducing this inflammation.”

In a double blind study, Dr. You and her colleagues randomized 11 obese patients, with an average body mass index of 34 kg/m2, insulin resistance, and vitamin D deficiency to vitamin D repletion therapy. Eight similar patients served as controls. The average age was 43 years.

Patients in the test group were placed on a step schedule for vitamin D supplementation. For 3 months, they received 40,000 IU of vitamin D3 weekly in an effort to reach a target 25-hydroxyvitamin D level of greater than 30 ng/ml. Patients then received another 3 months of the same supplementation with an aim to reach a target level of greater than 50 ng/ml.

“We wanted to see if there was a dose dependent effect for vitamin D in patients,” Dr. You said.

Endogenous glucose production decreased by 24% (P = .04) after normalization of vitamin D levels. Patients who received placebo saw an increase in endogenous glucose, pointing to lower hepatic insulin sensitivity, Dr. You said.

When the vitamin D receptors are activated, they inhibit the profibrotic pathways like TGFb-1, Dr. You explained, decreasing fibrosis.

The researchers also found a decrease in profibrotic gene expression in TGFb-1, HiF-1, MMP7, and Collagen I, V, and VI.

However, while testing for reduction in profibrotic gene expression in whole fat, the investigators found that there was no additional improvement after the first round of vitamin D therapy, leading them to assert that raising vitamin D levels above the normal range does not give any additional benefit.

ezimmerman@frontlinemedcom.com

On Twitter @eaztweets